Field
The present inventive concept relates to a composition effective for alleviating atopic dermatitis comprising extract of mixture of Undaria pinnatifida Sporophyll and ascidian shell and a method for manufacturing the composition.
Description of the Related Art
Atopic dermatitis not only includes skin inflammation, pigmentation, itching, etc. but also accompanies mental stress due to frequent recurrence which causes increase in time required for the treatment of atopic dermatitis. In addition, misdirected information on the treatment of atopic dermatitis causes distrust of the steroid treatment, and many are searching for secondary treatment or home remedy, which leads to serious inconvenience to patients and increase in cost for the treatment.
To treat atopic dermatitis, as the conventional remedies, substances such as ceramide, linoleic acid, vegetable oil or mineral oil, steroids such as hydrocortisone, formulations which add antibacterial and anti-inflammatory functions to steroids, the DNA synthesis inhibitor via ultraviolet therapy, hyperplastic cell inhibitors, inflammation and pruritus inhibitor have been proposed.
However, the steroid may lead to adverse side effects such as epidermal growth inhibition, and urea peroxide may lead to over-irritation to skin, and antibiotic substance such as antihistamines may lead to side effects such as tolerance of bacteria and photosensitivity disease.
The exact pathogenesis of atopic dermatitis is not yet fully understood, but it has been reported that immunological and non-immunological mechanism is involved along with genetic factors. Extrinsic atopic dermatitis which takes most part of atopic dermatitis is caused by immune mechanism associated with immunoglobulin E (IgE). It has been largely reported that delayed immunological reaction due to abnormal T-cells is more involved in extrinsic atopic dermatitis, rather than immediate immunological reaction toward allergen.
Further, these days, it has been reported that Th2-related cytokines such as interleukin (IL)-4 which generates the production of IgE from B cells causes atopic dermatitis. Therefore, the biggest problem with atopic dermatitis is increase in cytokines by rise in inflammatory reaction due to abnormal activation of the immune function.
In recent studies, it has been reported that, if proteinase-activated receptor-2 (PAR-2) which is protease-activation acceptor present in cell membrane is increased and activated, the mechanism in a cell, IκB kinase (IKK)→nuclear factor kappa B (NF-κB), is activated and increases inflammatory response, and as a result, various inflammatory materials such as cytokines (tumor necrosis factor (TNF)-α, IL-6, IL-10) cyclo-oxygenase (COX)-2, cytokine-inducible nitric oxide synthases (iNOS), adhesion molecules are increased, aggravating atopic dermatitis.
In other words, PAR-2 activation causes inflammation and pigmentation of the skin, itching, etc., and thus, suppression of PAR-2 activation is thought to be helpful in alleviating atopic dermatitis. According to recent studies, the PAR-2 inhibitors which are clinically used as a topical agent alleviate atopic dermatitis, and therefore, it is likely that PAR-2 inhibitors can be developed as a topical medication.